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10. Kelley GA, Kelley KS. Progressive resistance exercise and resting
blood pressure: a meta-analysis of randomized controlled trials. Hypertension 2000;35:838 – 43.
11. Quinn TJ. Twenty-four hour, ambulatory blood pressure responses
following acute exercise: impact of exercise intensity. J Hum Hypertens
2000;14:547–53.
12. Mahmud A, Feely J. Spurious systolic hypertension of youth: fit young
men with elastic arteries. Am J Hypertens 2003;16:229 –32.
13. Mottram PM, Haluska B, Yuda S, Leano R, Marwick TH. Patients
with a hypertensive response to exercise have impaired systolic function
without diastolic dysfunction or left ventricular hypertrophy. J Am
Coll Cardiol 2004;43:848 –53.
14. Kjeldsen SE, Mundal R, Sandvik L, Erikssen G, Thaulow E, Erikssen
J. Supine and exercise systolic blood pressure predict cardiovascular
death in middle-aged men. J Hypertens 2001;19:1343– 8.
15. Miyachi M, Kawano H, Sugawara J, et al. Unfavorable effects of
resistance training on central arterial compliance: a randomized intervention study. Circulation 2004;110:2858 – 63.
16. Missault L, Duprez D, de Buyzere M, de Backer G, Clement D.
Decreased exercise capacity in mild essential hypertension: non-invasive
indicators of limiting factors. J Hum Hypertens 1992;6:151–5.
17. Vanhees L, Defoor JG, Schepers D, et al. Effect of bisoprolol and
atenolol on endurance exercise capacity in healthy men. J Hypertens
2000;18:35– 43.
Appendix 1. Author Relationships With Industry and Others
Name
Research Grant
Astra Zeneca
Dr. Samuel S. Gidding
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Dr. Norman M. Kaplan
None
Scientific Advisory Board
Speakers’ Bureau
None
None
None
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None
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Boehringer Ingelheim
None
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Astra Zeneca
Aventis Pharmaceuticals
Bayer
BMS
Beechham
Eli Lilly & Co.
GlaxoSmithKline
Merck & Co.
Novartis Pharma AG
Pfizer
Phoenix Pharmaceuticals
Proctor & Gamble
Reliant Pharmaceutical
Solvay/Unimed
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None
Dr. Jackson T. Wright, Jr.
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Beechham
GlaxoSmithKline
Novartis Pharma AG
Phoenix Pharmaceuticals
Solvay/Unimed
None
●
●
Novartis Pharma AG
Pfizer
None
AstraZeneca
Bayer
Norvartis Pharma AG
Pfizer
Servier
●
Dr. Thomas G. Pickering
Steering Committee
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Beechham
GlaxoSmithKline
Phoenix Pharmaceuticals
Solvay/Unimed
Task Force 6: Coronary Artery Disease
Paul D. Thompson, MD, FACC, Chair
Gary J. Balady, MD, FACC, Bernard R. Chaitman, MD, FACC, Luther T. Clark, MD, FACC,
Benjamin D. Levine, MD, FACC, Robert J. Myerburg, MD, FACC
ATHEROSCLEROTIC CORONARY ARTERY DISEASE
General considerations. Compelling evidence indicates
that physical activity reduces cardiovascular events in
healthy subjects and cardiac mortality in patients with
diagnosed coronary artery disease (CAD) (1). Despite these
beneficial exercise effects, vigorous physical activity also
transiently increases the risk of both acute myocardial
infarction (AMI) (2– 4) and sudden cardiac death (SCD)
(5–7) with the greatest exercise risk among the most
habitually sedentary individuals (2,4,7).
Atherosclerotic CAD is the most frequent cause of these
exercise-related cardiac events in adults (8), variously defined as
older than 30, 35, or 40 years of age. Both plaque rupture
(9,10) and possibly plaque erosion (11) have been implicated as
the immediate cause of exercise-related events in adults, although plaque rupture is more frequent. Several studies over
the last decade document that cardiac events frequently occur
in coronary arteries that were not previously critically narrowed.
This appears to be particularly true for exercise-related cardiac
events because angiographic studies of exercise-related AMI in
the general population (4) and in sport participants (10)
demonstrate less extensive CAD than in comparison subjects.
This observation may reflect either selection bias for less severe
atherosclerosis in those capable of exercising at high intensity
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April 19, 2005:1348–53
or the ability of exercise to provoke events in individuals with
less severe disease.
Prognosis for diagnosed CAD patients worsens with the
extent of disease, left ventricular (LV) systolic dysfunction,
inducible ischemia, and electrical instability. Both the recognition that acute cardiac events often occur at the site of
previously mild coronary stenoses in the general population
and the observation that victims of exercise-related CAD
events have less extensive disease than do individuals suffering
non-exercise related events reduce the utility of standard CAD
risk assessment in evaluating older competitive athletes. Adolescent and young adult athletes also may have variants in their
resting electrocardiograms (ECGs) that make the interpretation of their resting and exercise ECGs difficult. In addition,
early CAD is increasingly identified by such imaging techniques as coronary artery calcification scoring, further complicating risk assessment because the presence of any coronary
artery calcification indicates atherosclerotic disease. Finally,
since CAD primarily occurs in adult athletes, the age of the
athlete at risk for CAD events complicates the decision
process. Older athletes are often engaged in individual competitive pursuits and may not require formal clearance for
continued competition. Preparticipation screening guidelines
specifically for participants in master’s sports have been developed in association with the American Heart Association
(AHA) (12).
Diagnosis. The diagnosis of atherosclerotic CAD is established in the presence of any of the following: 1) a history of
a myocardial infarction (MI) confirmed by conventional
diagnostic criteria; 2) a history suggestive of angina pectoris
with objective evidence of inducible ischemia; and 3) coronary atherosclerosis of any degree is demonstrated by
coronary imaging studies such as catheter-based coronary
angiography, magnetic resonance angiography, or electron
beam computerized tomography (EBCT).
CORONARY CALCIFICATION BY COMPUTED TOMOGRAPHY
Since the last version of these guidelines, the widespread dissemination of noninvasive techniques such as
EBCT, or even more recently, multi-slice gated CT, has
markedly increased the number of individuals, including
competitive athletes, who may be diagnosed with atherosclerotic CAD. Although exceedingly rare in young persons
(6% of men and 3% of women 20 to 29 years of age), the
presence of coronary calcium increases substantially with
age, such that for master’s athletes, age 40 to 49 years,
approximately 41% of men and 13% of women may have
measurable coronary calcium (13). Among individuals age
50 to 59 years, 68% of men and 27% of women have
documented coronary calcium (13). There is compelling
evidence that the presence of any coronary calcium indicates
underlying atherosclerosis (14) and that increasing coronary
calcium scores are associated with increased CAD risk (15).
The coronary calcium score that warrants additional evaluation in asymptomatic competitive athletes is unknown,
although scores of more than 100 (15) have been associated
(CT).
Thompson et al.
Task Force 6: Coronary Artery Disease
1349
with increased risk for coronary events (16) in the general
population compared to patients with no coronary calcium.
It is unknown whether the risk of coronary events during
intense exercise is increased in the presence of this or lesser
amounts of coronary calcium. Nevertheless, for the purpose
of the present document, athletes with coronary artery
calcification scores more than 100 should undergo the same
evaluation as those with more clinically evident CAD.
RISK ASSESSMENT. A paucity of data exists in competitive
athletes directly relating the presence and severity of CAD
to the risk of athletic participation. This requires that these
recommendations for athletes with CAD be based in part
on observations obtained from non-athletes with CAD.
Nevertheless, it is likely that risk is increased to some degree
whenever coronary atherosclerosis is present. It is also likely
that the risk of exercise-related events increases with the
extent of disease, LV dysfunction, inducible ischemia, and
electrical instability, and that the risk increases with the
intensity of the competitive sport and the intensity of the
participant’s effort.
Evaluation.
1. Athletes with CAD diagnosed by any method including
coronary artery classification scoring more than 100,
coronary angiography, evidence of inducible ischemia,
or prior coronary event, and who are undergoing evaluation for competitive athletics, should have their LV
function assessed.
2. These athletes should undergo maximal treadmill (or
bicycle) exercise testing to assess their exercise capacity
and the presence or absence of provocable myocardial
ischemia. Exercise testing should approximate as closely
as possible the cardiovascular and metabolic demands of
the planned competitive event and its training regimen.
Despite such simulation, graded exercise testing cannot
replicate the cardiovascular stress produced by the sudden bursts of activity, the combination of high dynamic
and static exercise, such as rowing, or the sustained
bouts of exercise required by athletic training and
competition. Therefore, standard clinical exercise tests
may not be appropriate for the evaluation of athletes
with coronary heart disease.
Two levels of risk can be defined on
the basis of testing.
Mildly increased risk. Athletes with CAD diagnosed by
any method are judged to be at mildly increased risk if they
demonstrate all of the following:
RISK STRATIFICATION.
1. Preserved LV systolic function at rest (i.e., ejection
fraction greater than 50%).
2. Normal exercise tolerance for age, demonstrated during
treadmill or cycle ergometer exercise testing: greater
than 10 metabolic equivalents (METS), or greater than
35 O2/kg-min if less than 50 years old; greater than 9
METS, or greater than 31 ml O2/kg-min for 50 to 59
years old; greater than 8 METS, or greater than 28 ml
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O2/kg-min, if 60 to 69 years old; and greater than 7
METS, or greater than 24 ml O2/kg-min, if greater
than or equal to 70 years old. It should be noted that
young, highly competitive endurance athletes should
have maximal oxygen uptakes far in excess of ranges
regarded as normal, which in fact may represent substantial functional impairment in this population.
3. Absence of exercise-induced ischemia and exerciseinduced or post-exercise complex ventricular arrhythmias, including frequent premature ventricular contractions (greater than 10% of beats/min), couplets, or
ventricular tachycardia.
4. Absence of hemodynamically significant stenosis (generally
regarded as 50% or more luminal diameter narrowing) in
any major coronary artery by coronary angiography.
5. Successful myocardial revascularization by surgical or
percutaneous techniques if such revascularization was
performed.
Substantially increased risk. Athletes with CAD identified by
noninvasive or invasive testing are judged to be at substantially increased risk if they demonstrate any of the following:
1. Impaired LV systolic function at rest (i.e., ejection
fraction less than 50%).
2. Evidence of exercise-induced myocardial ischemia or
complex ventricular arrhythmias.
3. Hemodynamically significant stenosis of a major coronary artery (generally regarded as 50% or more lumen
diameter narrowing) if coronary angiography was
performed.
The American College of Cardiology/AHA guidelines
on exercise testing note that it is not necessary to stop
beta-blockers before routine exercise testing, although this
practice may reduce the diagnostic and prognostic value of
the test (17). The decision whether or not to stop betablocker therapy before exercise testing of athletes should be
made on an individual basis. Stopping beta-blockers and
other anti-ischemic mediations before testing may be useful
to more closely approximate the probable risk if the athlete
either intentionally or unintentionally does not take these
medications before competition, or when certain athletic
regulatory bodies prohibit beta-blockers. If anti-ischemic
medications are stopped, this should be done carefully to
avoid a potential hemodynamic rebound effect, which could
lead to accelerated angina or hypertension.
Coronary arteriography is not required to determine
eligibility for competition in patients with known CAD,
and no evidence of inducible ischemia, but is recommended
in athletes with exercise-induced ischemia who choose to
participate in sports against medical advice. Such studies
may identify coronary lesions that may be better managed by
percutaneous or surgical myocardial revascularization procedures to relieve exercise-induced ischemia and potentially
to reduce exercise-related risk.
The panel wishes to emphasize that the following rec-
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April 19, 2005:1348–53
ommendations are prepared as a guidelines for permitting
participation in competitive sports. Restrictions in the following recommendations, therefore, should not be misinterpreted as an injunction against regular physical activity as
opposed to athletic competition. Indeed, regular and recreational physical activity and moderate-intensity exercise
training are recommended for patients with CAD for its
general cardiovascular benefits (1).
Recommendations:
1. Athletes in the mildly increased risk group can
participate in low dynamic and low/moderate static
competitive sports (classes IA and IIA—see Fig. 1 in
Task Force 8: Classification of Sports) but should
avoid intensely competitive situations. We recognize
that selected athletes with mildly increased risk may
be permitted to compete in sports of higher levels of
intensity when their overall clinical profile suggests
very low exercise risk. This is particularly true for
athletes in whom the only indication that coronary
atherosclerosis is present is from an EBCT performed for screening purposes, and in which the total
coronary calcium score is relatively low (i.e., less than
15). Increasing amounts of coronary calcium, suggestive of increasing burden disease, should dictate a
more cautious approach, particularly if the coronary
calcium score is more than 100. All athletes should
understand that the risk of a cardiac event with
exertion is probably increased once coronary atherosclerosis of any severity is present. Athletes with
mildly increased risk engaging in competitive sports
should undergo re-evaluation of their risk stratification at least annually.
2. Athletes in the substantially increased risk category
should generally be restricted to low-intensity competitive sports (class IA).
3. Athletes should be informed of the nature of prodromal symptoms (such as chest, arm, jaw and shoulder
discomfort, unusual dyspnea) and should be instructed to cease their sports activity promptly and to
contact their physician if symptoms appear. Physicians should be aware that competitive athletes may
minimize symptoms that occur during exertion.
4. Those with a recent MI or myocardial revascularization should cease their athletic training and competition until recovery is deemed complete. This interval varies among patient groups, but depends on the
severity of the cardiovascular event and the extent
and success of the revascularization procedure. Such
patients may benefit from cardiac rehabilitation during the recovery period. No firm guidelines exist for
how long patients should avoid vigorous exercise
training, but in general, patients post-stent placement for stable CAD symptoms should avoid vigorous exercise training for competition for approximately four weeks. Patients undergoing stent
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Task Force 6: Coronary Artery Disease
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placement for unstable disease should wait at least
this long. Following coronary bypass surgery, patients should avoid vigorous training until their
incisions can tolerate vigorous activity. After recuperation period, the risk and activity level should be
defined as in recommendations 1 and 2.
5. All athletes with atherosclerotic CAD should have
their atherosclerotic risk factors aggressively treated
as studies suggest that comprehensive risk reduction
is likely to stabilize coronary lesions and may reduce
the risk of exercise-related events.
evaluation and risk stratification approach delineated
for athletes with coronary atherosclerosis.
2. Athletes with coronary vasospasm documented at rest
or with exercise and angiographically normal coronary
arteries or without evidence of arterial plaquing should
be restricted to low-intensity competitive sports (class
IA). This restriction should be re-evaluated at least
annually because some patients with coronary vasospasm may experience spontaneous remission.
It must be emphasized that even athletes identified as
being at mildly increased risk and permitted to participate in
low dynamic and low/moderate static competitive sports
(classes IA and IIA) cannot be assured that such participation will not increase the risk of cardiac events because it is
probable that any exercise transiently poses some increased
exercise risk once CAD is established.
CAD IN CARDIAC TRANSPLANT RECIPIENTS
CORONARY ARTERY VASOSPASM
Coronary artery vasospasm classically presents as rest angina
associated with ST-segment elevation, but can be provoked
by physical exertion on rare occasions (18). Vasospasm is an
uncommon cause of chest pain that is evident in 2% to 3%
of patients presenting with chest pain undergoing coronary
angiography (19). Vasospasm is most frequently observed at
coronary sites damaged by atherosclerosis (20), but a substantial cohort may have angiographically normal coronary
arteries or minimal angiographic luminal narrowing (18,19).
A vasospastic contribution to ischemia should be suspected
when there is marked variation in the exercise threshold for
angina (18), and when there is evidence of myocardial
ischemia with little or no coronary luminal narrowing.
Presently, no widely accepted noninvasive test exists for
eliciting and quantifying vasospastic angina in the setting of
nonobstructive or mildly obstructive coronary arteries. The
occurrence of ST-segment elevation during exercise testing
appears to correlate with the degree of disease activity (i.e.,
those with more frequent episodes of angina will more likely
have a positive test) (21). Provocative testing with
ergonovine-related substances during coronary arteriography is rarely used (22), but remains the only test recommended in current practice guidelines (23). However, forced
hyperventilation testing, particularly when combined with
nuclear perfusion imaging, may be a useful noninvasive test
not requiring the administration of ergonovine (24). The
risk associated with participation in sports for athletes with
coronary artery spasm is not known, but we recommend a
cautious approach to patients with documented coronary
vasospasm until the risk of physical exertion for these
patients is better defined.
Recommendations:
1. Athletes with CAD as previously defined and clinically
important coronary artery vasospasm should follow the
Orthotopic transplanted hearts develop an accelerated form
of coronary vasculopathy, usually detected by serial coronary
angiography or intravascular ultrasound studies, that is a
leading cause of death after the first post-transplant year
(25,26). The coronary disease is different from that seen in
non-transplanted hearts with coronary atherosclerosis; the
disease is diffuse and characterized by pronounced intimal
thickening and involvement of the entire coronary tree.
Discrete stenoses of epicardial arteries can coexist in some
instances. Cardiac allografts are denervated, and although
some recipients may develop a degree of sympathetic reinnervation, acute coronary syndromes may present with
atypical symptoms as opposed to angina (27). Noninvasive
testing for CAD is less sensitive in the transplant recipient;
many patients do not achieve VO2max, and cardiac denervation can limit peak heart rate response and symptoms.
Provocative myocardial perfusion imaging can fail to detect
ischemia (25,27) although dobutamine echocardiography
has been shown to predict subsequent ischemic cardiac
events (26,28 –31) after the first three to five years posttransplant. In many cardiac transplant centers, a normal
stress echocardiogram justifies postponement of annual
coronary angiography (26,28 –31). Coronary angiography
can also underestimate disease severity because of the diffuse
nature of the CAD process; intravascular ultrasound studies
increase the sensitivity (26).
Evaluation.
1. Cardiac transplant recipients participating in competitive athletics should undergo yearly maximal exercise
testing with echocardiography using a protocol designed
to simulate the cardiac and metabolic demands of the
competitive event and its training.
2. Additional evaluation, including such procedures as
coronary angiography and intravascular ultrasonography
(IVUS) should be performed as directed by the transplant center and the transplant cardiologist. Coronary
angiography/IVUS should also be performed if the
annual exercise test is abnormal and to evaluate unexplained symptoms such as dyspnea or exertional fatigue
as these may be the only symptoms of progressive
vascular disease.
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Task Force 6: Coronary Artery Disease
Recommendations:
1. Because of the special issues involved with transplant
patient management, decisions as to the feasibility of
athletic competition for cardiac transplant recipients
should be made in conjunction with the patient’s
transplant cardiologist.
2. Athletes with no coronary luminal narrowing, no
exercise-induced ischemia, and with normal exercise
tolerance for age (as previously defined ) can generally participate in all competitive sports as appropriate for their exercise capacity.
3. Athletes with coronary luminal narrowing should be
risk stratified as outlined in the section entitled
Evaluation with activity recommendations as indicated in the section entitled Atherosclerotic Coronary Artery Disease.
MYOCARDIAL BRIDGING
Myocardial bridging is a condition in which a segment of
major epicardial coronary artery (most commonly the left
anterior descending) is tunneled within and completely
surrounded by LV myocardium. Myocardial bridging is
found in approximately 30% of hearts examined at necropsy
(32), but is visualized during angiography in less than 5% of
patients probably because the thin bridges identified at
necropsy cause little anatomic compression during systole
(32). Consequently, most tunneled epicardial coronary arteries appear to be of little clinical significance, but this
malformation has occasionally been associated with
exercise-related sudden death (33,34) and exercise-induced
angina pectoris (35). Clinically significant myocardial
bridges have a long deeply-tunneled segment and are
associated with regional ischemia. Treatment options include medical management with beta-adrenergic or calcium
channel-blocking agents, coronary stenting, and surgical
resection of the myocardial bridge.
However, coronary stenting has been associated with
restenosis and periprocedural complications in 50% of cases
(32). Surgical resection in selected symptomatic patients has
been shown to reduce angina (35) and improve myocardial
blood flow (36). Task Force 4: HCM and Other Cardiomyopathies, Mitral Valve Prolapse, Myocarditis, and
Marfan Syndrome provides recommendations for the management of myocardial bridging in patients with hypertrophic cardiomyopathy (HCM).
Recommendations:
1. Athletes with myocardial bridging of an epicardial
coronary artery and no evidence of myocardial ischemia at rest or during exercise can participate in all
competitive sports as appropriate for their exercise
capacity.
2. Athletes with myocardial bridging of an epicardial
coronary artery and objective evidence of myocardial
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April 19, 2005:1348–53
ischemia or prior MI should be restricted to lowintensity competitive sports (class IA).
3. Athletes with surgical resection of the myocardial
bridge or stenting should be restricted to lowintensity sports for at least six months after the
procedure. Athletes who remain asymptomatic after
the procedure should undergo exercise testing. If
exercise tolerance is normal for age and gender, and
there is no evidence of exercise-induced ischemia, the
athlete may participate in all competitive sports.
Finally, recommendations for other congenital coronary
artery anomalies, including those originating from the
wrong coronary sinus, are provided in Task Force 1:
Preparticipation Screening and Diagnosis of Cardiovascular
Disease in Athletes.
doi:10.1016/j.jacc.2005.02.013
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Appendix 1. Author Relationships With Industry and Others
Name
Research
Grant
Consultant
Dr. Gary J. Balady
None
Dr. Bernard R. Chaitman
●
CV Therapeutics
None
●
●
Aventis
Pfizer
Scientific
Advisory Board
None
●
●
Aventis
CV Therapeutics
Speakers’
Bureau
None
●
Pfizer
Stock
Holder
Expert Witness
Testimony
None
None
None
None
Dr. Luther T. Clark
None
None
None
None
None
None
Dr. Benjamin D. Levine
None
None
None
None
None
None
Dr. Robert J. Myerburg
●
●
None
●
●
None
None
●
Guidant
Procter & Gamble
Procter & Gamble
Reliant
Pharmaceutical
●
●
Dr. Paul D. Thompson
●
●
Astra Zeneca
Bristol Myers
Squibb
●
●
●
●
Astra Zeneca None
Merck
Pfizer
Schering
●
●
●
●
Astra Zeneca
Merck
Pfizer
Schering
●
●
Pfizer
Schering
●
●
●
●
●
2000, Defense, Lewis vs.
Mudge
2002, Defense, Weiner
vs. Vitello
2005, Defense, Ephedra
Multi-District Litigation
2005, Plaintiff, Sudden
death in college athlete
2004, Defense, Stress
test/recreational sports
2002, Sudden death,
World Gym
2002, Plaintiff, Sudden
death, truck driver
1998, Plaintiff, Sudden
death, recreational sports